Maritide (MariTide): A GIPR-Antagonist GLP-1-Agonist Bispecific for Obesity

This content is provided by Superpower Health for educational and informational purposes only. Superpower Health does not prescribe, sell, or facilitate access to maritide (maridebart cafraglutide). Maritide is an investigational compound not FDA-approved for any indication. It is not available through Superpower or by prescription outside of clinical trials. This page is not a substitute for medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider.

The incretin pharmacology field has been built on one organizing principle: that stimulating GLP-1 receptors reduces appetite and body weight, and that adding GIP receptor activity makes that effect stronger. Tirzepatide validated that principle at scale. But a competing hypothesis has been gaining traction, and it inverts the GIP logic entirely. What if blocking GIP receptor signaling, rather than activating it, amplifies GLP-1-driven weight loss even further?

Maritide (also known as maridebart cafraglutide) is the most advanced clinical test of that hypothesis. Developed by Amgen under the code name AMG 133, Maritide pairs a GIP receptor antagonist antibody with two GLP-1 receptor agonist peptides in a single molecule, and it is dosed monthly rather than weekly. This article covers how maritide is engineered, what the Phase 1 and Phase 2 data show, the scientific debate at the center of its mechanism, and where it stands in the regulatory process as of April 2026.

Key Takeaways

• Regulatory Status: Not FDA-approved as of April 2026. Investigational compound; Phase 3 MARITIME trials initiated 2024/2025. Not available through Superpower or by prescription.
• Research Stage: Phase 1 and Phase 2 randomized controlled trials completed and published; Phase 3 program (MARITIME) ongoing.
• Availability: Available only through clinical trial enrollment. Superpower does not offer this compound. For current trial listings, see ClinicalTrials.gov.
• Compound reference: IUPHAR/BPS Guide to PHARMACOLOGY: maridebart cafraglutide (ligand 13316)
• How it works: Blocks GIP receptors via an antibody component while simultaneously activating GLP-1 receptors via two conjugated peptide agonists.
• What the research shows: Phase 2 trial in 592 adults showed 12-16% placebo-subtracted weight reduction at 52 weeks with once-monthly dosing; Phase 1 data showed weight loss maintained for up to 150 days after the last dose.

What Maritide Is and How It Was Engineered

Origin and molecular architecture

Maritide originated from Amgen's program to test whether antagonizing the GIP receptor, rather than activating it, could enhance the weight-reducing effects of GLP-1 receptor agonism. The foundational preclinical work was published in 2018 in Science Translational Medicine by Killion, Wang, Yie, and colleagues from Amgen Research. That study demonstrated that GIPR antagonist antibodies reduced body weight and improved multiple metabolic parameters in diet-induced obese mice and non-human primates, with effects that were further amplified when the GIPR antibody was combined with a GLP-1 receptor agonist in the same preclinical models. The implication was that these two mechanisms could be more effective together than either alone. The challenge was engineering a single molecule that preserved both activities while achieving the long plasma half-life needed for monthly dosing. A 2026 medicinal chemistry paper in Journal of Medicinal Chemistry by Wu and colleagues described in detail how AMG 133 was engineered by conjugating synthetic GLP-1 peptides to IgG-based anti-GIPR antibodies using amino acid linkers, resulting in a structure that markedly prolonged GLP-1 peptide exposure compared with unconjugated analogs.

The bispecific structure

Maritide's architecture is unusual in the GLP-1 class. Most incretin drugs are either small peptide analogs (semaglutide, tirzepatide) or small molecules (orforglipron). Maritide is an antibody-drug conjugate: a full-length IgG-class anti-GIPR monoclonal antibody with two GLP-1 receptor agonist peptides attached via linkers, one to each heavy chain. The foundational characterization of this structure was published in 2024 in Nature Metabolism by Veniant, Lu, and colleagues. That paper confirmed dual receptor activity in cell-based systems, described the antibody-peptide conjugate architecture, and presented preclinical weight loss data in obese mice and cynomolgus monkeys alongside the first Phase 1 human data. The antibody backbone confers a long half-life that supports monthly subcutaneous dosing, an interval substantially less frequent than the weekly injections required by semaglutide and tirzepatide. A previous precedent for long-acting antibody-linked GLP-1 pharmacology was dulaglutide, an Fc-fused GLP-1 analog described in 2010 in Diabetes and Metabolic Research and Reviews by Glaesner and colleagues, which established that appending GLP-1 analogue peptides to an antibody scaffold was clinically viable and could extend receptor engagement beyond what native GLP-1 peptide half-lives permit. Maritide advances this approach by combining the antibody scaffold with a second, antagonist function at a separate receptor.

What GIP actually does in the body

Any discussion of GIPR antagonism requires a prior understanding of GIP itself. GIP (glucose-dependent insulinotropic polypeptide) is an incretin hormone whose actions extend well beyond the pancreas. A 2023 review in Nature Reviews Endocrinology by Hammoud and Drucker, one of the defining figures in incretin biology, detailed the contrasting cardiometabolic actions of GIP and GLP-1 across adipose tissue, brain, and cardiovascular systems, providing an authoritative reference point for how GIP signaling differs from GLP-1 signaling in peripheral and central tissues. A 2025 consensus review in Molecular Metabolism by Muller and roughly thirty other leaders in incretin science synthesized GIP's roles in adipose, bone, central nervous system, and pancreatic biology, framing GIP not as a single-tissue hormone but as a pleiotropic regulator of energy balance. These references establish the biological complexity that any GIPR-modulating therapy, whether agonist or antagonist, must contend with.

The GIPR paradox: why blocking GIP may work

The most scientifically contested aspect of maritide's design is the choice to antagonize rather than activate the GIP receptor. Tirzepatide is a GIP receptor agonist combined with a GLP-1 receptor agonist, and it produces among the largest weight reductions of any approved pharmacotherapy. Maritide does the opposite on the GIP arm and achieves similar-magnitude results. This apparent paradox has generated substantial debate in incretin biology. A 2025 review in Diabetes by Campbell revisited the long-standing agonism-versus-antagonism controversy and synthesized why both directions of GIPR modulation appear to reduce body weight, offering what is arguably the cleanest published encapsulation of the paradox.

One proposed resolution involves receptor desensitization. A 2020 paper in Nature Communications by Killion, Chen, Falsey, and colleagues from Amgen demonstrated in mechanistic experiments that chronic GIP receptor agonism desensitizes adipocyte GIPR activity, effectively producing functional receptor downregulation that may mimic the metabolic consequences of antagonism. Under this model, chronic agonism and direct antagonism converge on similar downstream states. Human genetics provides independent evidence on the antagonism side: a 2024 study in Nature Metabolism by Kizilkaya and colleagues performed functional characterization of loss-of-function GIPR variants in large population datasets and found that naturally occurring GIPR loss-of-function variants are associated with lower BMI, providing human genetic validation that reducing GIP receptor activity correlates with reduced adiposity. A 2024 review in Trends in Endocrinology and Metabolism by Novikoff and Muller synthesized the preclinical and human evidence, framing the science as supporting the idea that antagonizing GIPR amplifies GLP-1 receptor-driven weight loss by preventing GIP-mediated attenuation of GLP-1 signaling at shared downstream nodes.

The case for GIP receptor agonism was articulated in a 2025 review in Diabetes by Samms and Sloop, who argued that GIPR agonism improves metabolic health through beneficial effects in pancreatic islets, the central nervous system, and adipose tissue, making agonism the better-supported therapeutic direction. A neutral synthesis was provided by a 2025 review in Journal of Clinical Medicine by Douros, Mowery, Knerr, and colleagues, which examined evidence for both GIPR agonist and GIPR antagonist programs side by side and concluded that both approaches reduce body weight through different mechanisms, neither of which has been definitively shown to be superior. The resolution to this debate likely depends on circuit-level neuroanatomy: a 2025 mouse study in Nature Metabolism by Gutgesell and colleagues, from the Muller and Tschop laboratory, independently showed that GIPR agonism and antagonism reduce body weight through distinct neuronal circuits, suggesting that the two strategies are not equivalent at a biological level even if they converge on similar body weight outcomes in some preclinical models.

GIPR in the brain: how blocking GIP reduces food intake

Maritide's appetite-suppressing effects are unlikely to be explained by adipose or pancreatic action alone. A 2024 review in Peptides by Liskiewicz focused on central GIPR signaling and described the role of brain GIP receptors in energy balance, arguing that GIPR expression in the hypothalamus and hindbrain is integral to GIP's effects on body weight. A 2025 review in Frontiers in Endocrinology by James-Okoro and colleagues expanded on that picture by synthesizing hypothalamic and hindbrain mechanisms by which GIPR modulation influences food intake control, bridging the gap between receptor pharmacology and eating behavior. At a more granular level, a 2023 primary research paper in JCI Insight by Adriaenssens and colleagues identified distinct hypothalamic and brainstem GIPR neuron populations with different roles in feeding behavior, providing neural-circuit evidence that GIPR modulation acts on defined appetite-regulatory nuclei rather than through diffuse central effects. Together, these references support the view that maritide's GIPR-blocking arm engages central appetite circuits alongside its peripheral metabolic actions.

What the Human Evidence Shows

Phase 1 trial and the post-dose weight maintenance signal

The first Phase 1 human data for maritide were reported alongside the preclinical mechanistic data in the 2024 Nature Metabolism publication by Veniant, Lu, and colleagues. The Phase 1 trial (NCT04478708) was a randomized, double-blind, placebo-controlled single and multiple ascending dose study in adults aged 18-65 with obesity and without diabetes, evaluating single doses from 21 mg to 840 mg and multiple-dose regimens. In the highest multiple-ascending-dose cohort, AMG 133 produced approximately 14.5% mean body weight reduction by day 85 compared with approximately 1.5% in the placebo arm, with lower doses producing roughly 7.4% reductions after three doses. The clinically notable finding was that weight loss was maintained for up to 150 days after the last dose in multiple cohorts, a pattern markedly different from the rapid weight regain observed after stopping semaglutide or tirzepatide. Adverse events were predominantly mild, transient gastrointestinal symptoms (nausea, vomiting) that resolved within approximately 48 hours of dosing, with no treatment-related serious adverse events or discontinuations reported; the small Phase 1 sample and short duration limit generalizability. Whether this durable post-dose signal reflects maritide's long pharmacokinetic half-life, a persistent receptor-level or central adaptation, or some combination of the two remains under investigation. The sustained effect was highlighted in a 2024 research commentary in Nature Reviews Endocrinology by Greenhill, who framed the durable post-dose weight-loss signal as clinically significant given what is known about weight regain trajectories after GLP-1 agonist discontinuation.

Phase 2 trial: efficacy in 592 adults

The pivotal Phase 2 data were published in September 2025 in The New England Journal of Medicine by Jastreboff, Ryan, Bays, Ebeling, and colleagues. That trial randomized 592 adults across two cohorts. The first cohort enrolled 465 participants with obesity but without type 2 diabetes. The second enrolled 127 participants with obesity and type 2 diabetes. All participants were treated with once-monthly maridebart cafraglutide or placebo for 52 weeks.

In the obesity-without-diabetes cohort (n = 465, roughly 67 placebo, 99 per active arm at 140 and 280 mg, and 133 in the 420 mg escalation group), mean body weight reductions at 52 weeks ranged from −12.3% (95% CI, −15.0 to −9.7) to −16.2% (95% CI, −18.9 to −13.5) with maridebart cafraglutide (tested at 140, 280, and 420 mg subcutaneously every 4 weeks) versus −2.5% (95% CI, −4.2 to −0.7) with placebo, producing placebo-subtracted reductions of approximately 9.8 to 13.7 percentage points. The weight-loss trajectory had not yet reached a plateau at 52 weeks across all tested doses, suggesting continued weight-reduction potential beyond the trial window. In the obesity-with-type-2-diabetes cohort (n = 127, approximately 32 per arm under 1:1:1:1 randomization), mean body weight reductions ranged from −8.4% (95% CI, −11.0 to −5.7) to −12.3% (95% CI, −15.3 to −9.2) versus −1.7% (95% CI, −2.9 to −0.6) with placebo (placebo-subtracted 6.7 to 10.6 percentage points), accompanied by HbA1c reductions of 1.2 to 1.6 percentage points versus a 0.1 percentage-point increase with placebo. These HbA1c improvements reflect GLP-1 receptor agonism's established mechanism of enhancing glucose-dependent insulin secretion while reducing glucagon secretion. Cohort-level p-values versus placebo were not reported in the abstract and the small per-arm T2D sample size limits the precision of effect estimates in that cohort.

The most common adverse events in the Phase 2 trial were gastrointestinal: nausea, vomiting, and constipation, consistent with GLP-1 receptor agonist pharmacology. Two published letters in The New England Journal of Medicine in December 2025 raised methodological questions about the trial. Liu discussed the interpretation of the weight-loss trajectory and safety findings, while Muskiet and Smits raised methodological questions about GI tolerability and discontinuation. Jastreboff, Ryan, and Pannacciulli responded directly to those critiques, addressing the tolerability and trajectory questions in detail. The debate reflects the scientific scrutiny appropriate for a compound at this stage of development and does not alter the primary efficacy findings of the Phase 2 publication.

Positioning within the incretin landscape

The 52-week Phase 2 weight loss range for maritide (approximately 12-16% placebo-subtracted in the obesity-without-diabetes cohort) is broadly comparable to GLP-1 monotherapy benchmarks and approaches tirzepatide at some doses. For context, the STEP 1 Phase 3 trial of once-weekly semaglutide 2.4 mg, published in 2021 in The New England Journal of Medicine by Wilding, Batterham, and colleagues, randomized 1,961 adults with overweight or obesity without diabetes 2:1 to semaglutide versus placebo and demonstrated approximately 14.9% mean weight loss versus 2.4% with placebo at 68 weeks (p < 0.001). The SURMOUNT-1 Phase 3 trial of tirzepatide, published in 2022 in The New England Journal of Medicine by Jastreboff, Aronne, Ahmad, and colleagues, enrolled 2,539 adults with obesity or overweight with comorbidities and demonstrated mean weight loss of approximately 15.0%, 19.5%, and 20.9% at the 5 mg, 10 mg, and 15 mg weekly doses at 72 weeks, respectively, versus 3.1% with placebo (p < 0.001 for all doses versus placebo). The retatrutide Phase 2 trial, testing a triple GLP-1/GIP/glucagon receptor agonist and published in 2023 in The New England Journal of Medicine by Jastreboff, Kaplan, Frias, and colleagues, reported up to 24.2% weight reduction at 48 weeks at the highest tested dose. Cross-trial comparisons are unreliable due to differences in study design, patient populations, treatment duration, and dosing strategies. These figures are presented for scientific context only; these compounds have fundamentally different regulatory statuses and evidence bases. A 2026 high-impact review in Endocrine Reviews by Son and colleagues surveyed novel GLP-1-based medications including dual agonists, tri-agonists, and antibody conjugates like maritide, situating the compound within the broader competitive landscape of next-generation obesity pharmacotherapy.

Maritide's monthly dosing interval remains its most distinctive practical feature. Weekly subcutaneous injection is a meaningful compliance burden for many patients. Whether monthly dosing improves adherence and real-world outcomes in the Phase 3 program is one of the key questions the MARITIME trials are designed to answer.

Regulatory and Legal Status

FDA classification and current trial status

As of April 2026, maritide (maridebart cafraglutide / AMG 133) is not FDA-approved for any indication. It is classified as an investigational new drug (IND) under active Phase 3 clinical development. The Phase 3 MARITIME program was initiated by Amgen in 2024 and 2025 across multiple trial arms, including populations with obesity, with type 2 diabetes, and with cardiometabolic comorbidities. Maritide is not available through compounding pharmacies, is not available by prescription outside of clinical trial protocols, and is not available through Superpower. The compound has no approved NDA or BLA as of April 2026.

What would need to change for maritide to become available

For maritide to receive FDA approval and become available by prescription, Amgen would need to submit a New Drug Application (NDA) or Biologics License Application (BLA) based on completed Phase 3 data from the MARITIME program, and the FDA would need to review and approve that submission. Phase 3 trials typically require 2-5 years to complete and analyze. NDA review adds 10-12 months on the standard pathway or 6 months under Priority Review if the FDA grants that designation. Based on publicly available information about MARITIME trial initiation timelines, FDA approval before 2028 would be optimistic, and no approval timeline can be guaranteed. Until an approval is granted, maritide remains available only to participants enrolled in active clinical trials.

What this means practically

Products labeled as maritide, AMG 133, or maridebart cafraglutide available from online vendors or gray-market sources are not regulated by the FDA and have not been evaluated for identity, purity, or potency. The compound is proprietary to Amgen; no legitimate compounded version exists. Individuals interested in access should monitor ClinicalTrials.gov for open enrollment in the MARITIME program or related studies.

Comparators and Context

Maritide is most directly compared to tirzepatide (Mounjaro, Zepbound), the only currently FDA-approved compound that also targets the GIP receptor. The mechanism difference is stark: tirzepatide is a GIP receptor agonist, while maritide is a GIP receptor antagonist. Both produce meaningful weight loss, and the clinical data do not yet establish which approach is superior at the mechanism level. The debate is genuine and ongoing in the incretin biology literature, with Lilly researchers having published arguments for the agonism approach and independent groups providing evidence that both antagonism and agonism can reduce body weight through distinct circuits. A 2026 head-to-head preclinical study in male mice by Davies, Turland, Tran, and colleagues, published in Diabetes, Obesity and Metabolism, confirmed that both GIPR agonism and antagonism produce metabolic benefits in preclinical models, with different metabolic signatures. This comparison is for scientific context only; tirzepatide is an FDA-approved prescription medication with an established clinical evidence base, while maritide is an investigational compound with no approved indication.

The weight regain question also distinguishes maritide from current standards of care. Evidence from approved compounds is consistent: weight returns substantially after discontinuation. The STEP 1 extension study, published in 2022 in Diabetes, Obesity and Metabolism by Wilding, Batterham, Davies, and colleagues, showed that participants regained approximately two-thirds of their prior weight loss within one year of stopping semaglutide. SURMOUNT-4, published in 2024 in JAMA by Aronne, Sattar, Horn, and colleagues, showed that discontinuing tirzepatide after an initial 36-week treatment period resulted in substantial weight regain, with continued treatment maintaining loss far more effectively than placebo. Phase 1 data for maritide suggested weight maintenance for up to 150 days after the last dose, a pattern that has not been documented at this duration for weekly GLP-1 agonists. A 2026 review in Diabetes, Obesity and Metabolism by Shah and colleagues surveyed the clinical management of weight regain and cardiometabolic consequences after GLP-1 receptor agonist discontinuation, underscoring that long-term therapy planning is itself becoming a distinct clinical consideration for this drug class. Whether maritide's post-dose durability translates to a clinically meaningful advantage in Phase 3 populations requires confirmation in the MARITIME trials.

Safety: What Is and Is Not Known

Phase 1 and Phase 2 safety data

The safety profile reported across Phase 1 and Phase 2 maritide trials has been consistent with GLP-1 receptor agonist pharmacology. The most common adverse events are gastrointestinal: nausea, vomiting, and constipation. These effects are dose-dependent and were reported to diminish with dose escalation strategies that allow the body to accommodate increasing GLP-1 receptor activity gradually. No unexpected safety signals have been identified in published Phase 1 or Phase 2 data. The Phase 2 trial did not report serious adverse events attributable to the compound that distinguished maritide from the known GLP-1 class profile. A 2026 review in Metabol Open of multi-receptor agonists and next-generation metabolic modulators confirmed that maritide's adverse-event profile in published trials has been predominantly mild-to-moderate GI events, consistent with the broader class.

What remains unknown

Long-term safety data in large populations do not yet exist. Phase 2 trials are designed to assess efficacy and detect safety signals, not to characterize the full long-term risk profile of a compound. Cardiovascular outcomes, effects on bone, renal function, and cancer risk all require Phase 3 data and post-marketing surveillance to evaluate fully. The antibody component of maritide's structure raises considerations specific to biologic drugs, including potential immunogenicity (antibody formation against the therapeutic antibody), which has been monitored in trials but requires long-term follow-up for full characterization. The GLP-1 receptor agonist class carries an FDA-mandated warning about thyroid C-cell tumors based on rodent studies; maritide's GLP-1 peptide component makes this a relevant safety consideration, and clinical trials will monitor thyroid biomarkers accordingly. Providers and patients evaluating trial enrollment should review the current MARITIME trial consent documentation for the full investigational risk disclosure.

Who Should Not Use Maritide

Because maritide is investigational, contraindications are defined by clinical trial eligibility criteria rather than an approved prescribing label. Based on the compound's mechanisms, the following groups face elevated theoretical risk and would typically be excluded from or face additional scrutiny in trial enrollment:

• Personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2), given the GLP-1 receptor agonist component and the class-associated thyroid C-cell signal in rodent models
• Active malignancy, particularly tumors with GLP-1 or GIP receptor expression, given the theoretical concern that receptor-modulating agents might affect tumor biology
• Severe or uncontrolled gastroparesis, as GLP-1 receptor agonism slows gastric motility and may worsen this condition
• History of serious hypersensitivity to biologic therapeutics, given maritide's antibody-drug conjugate structure
• Pregnancy and breastfeeding, as safety in these populations has not been established and weight loss pharmacotherapy is generally not indicated during pregnancy
• Severe renal or hepatic impairment, as pharmacokinetic data in these populations are limited

Eligibility for trial enrollment is determined by the clinical trial investigators based on the specific protocol's inclusion and exclusion criteria, not by this list. Individuals interested in MARITIME trial participation should consult the official trial documentation at ClinicalTrials.gov.

Which Biomarkers Are Relevant if You Are Exploring Metabolic Therapy?

Understanding your metabolic baseline is a reasonable step regardless of which therapeutic approaches are accessible. Maritide targets interconnected metabolic systems, and the markers below reflect the biology the compound engages. Establishing these baselines provides objective data that informs conversations with a provider, regardless of whether maritide becomes available to you.

• HbA1c (glycated hemoglobin): Reflects average blood glucose over approximately 90 days. Maritide's GLP-1 receptor agonist component enhances glucose-dependent insulin secretion and reduces glucagon; the Phase 2 trial showed meaningful HbA1c reductions in the type 2 diabetes cohort. Baseline HbA1c establishes glycemic status before any metabolic intervention.
• Fasting glucose: Direct measure of glycemic control at the point of testing. Relevant for assessing insulin resistance, pre-diabetes status, and monitoring the glycemic effects of any GLP-1 receptor-active compound.
• Fasting insulin: Elevated fasting insulin relative to fasting glucose is a sensitive early marker of insulin resistance. Because maritide acts partly through enhancing insulin secretion efficiency, insulin baseline and response can contextualize glycemic changes during any incretin-based intervention.
• Triglycerides: GLP-1 receptor agonists reduce hepatic triglyceride output and improve postprandial lipemia. Baseline triglycerides establish the lipid environment before any metabolic therapy and allow quantification of any intervention's cardiometabolic effects.
• Body weight, BMI, and waist circumference: Foundational anthropometric baselines for any weight-loss intervention. Phase 2 trial outcomes were expressed as percent reduction from baseline weight, so having a precise baseline is essential for interpreting any future data on one's own trajectory.
• hs-CRP (high-sensitivity C-reactive protein): A sensitive marker of systemic inflammation. Metabolic disease is frequently accompanied by low-grade chronic inflammation, and weight reduction is associated with reductions in hs-CRP. Baseline hs-CRP provides context for tracking the cardiometabolic benefit of any metabolic intervention.
• Lipid panel (LDL, HDL, total cholesterol): Obesity and insulin resistance frequently co-occur with dyslipidemia. GLP-1 receptor agonist pharmacotherapy is associated with modest reductions in LDL and triglycerides. Baseline lipid values allow tracking of cardiometabolic improvement alongside weight change.

The Bottom Line

Maritide represents a genuinely novel approach within the incretin class. Its antibody-peptide conjugate structure, monthly dosing interval, and GIP receptor antagonism all distinguish it from approved GLP-1 therapies, and the Phase 1 signal of extended post-dose weight maintenance has not been replicated at that duration with weekly GLP-1 agonists. Phase 2 data in 592 participants confirmed meaningful weight reduction over 52 weeks with a safety profile consistent with the GLP-1 class. Whether those results are durable and whether superiority to existing approved options can be established will require the Phase 3 MARITIME program to read out. As of April 2026, maritide is not approved, is not available by prescription, and is not available through Superpower. Understanding your own metabolic biomarkers is a reasonable step regardless of which specific therapeutic options become accessible to you or your provider.

That principle is central to Superpower's approach to preventive health: objective biomarker data should precede and inform every clinical decision, whether the compound in question is available today or still working through regulatory review. Knowing your HbA1c, fasting glucose, insulin, and lipid baseline before any metabolic intervention gives you and your provider the clearest possible picture of where you are starting and what is changing.

IMPORTANT SAFETY INFORMATION

Maritide (maridebart cafraglutide / AMG 133) is not FDA-approved for any indication as of April 2026. It is an investigational new drug in the Phase 3 MARITIME program under Amgen's active IND. Maritide is not a Category 2 bulk drug substance under FDA Section 503A and has not been reviewed for compounding eligibility; its antibody-peptide conjugate structure is not reproducible through standard compounding pathways, and it is not eligible for compounding under 503A or 503B. Access is restricted to participants enrolled in authorized, IRB-approved clinical trials. Superpower is a technology platform; Superpower does not prescribe, sell, compound, or facilitate access to maritide or any investigational compound. This page is provided for educational and informational purposes only and does not constitute medical advice.

Maritide is not available by prescription, is not available from compounding pharmacies, and is not sold or offered by Superpower. Any online product claiming to be maritide, AMG 133, or maridebart cafraglutide has not been approved or evaluated by the FDA.

Warnings: The GLP-1 receptor agonist class, including compounds like maritide that contain a GLP-1 agonist component, carries FDA safety communication regarding thyroid C-cell tumors observed in rodent studies. The clinical relevance in humans is not established but is monitored in clinical trials. GLP-1 receptor agonist compounds are associated with gastrointestinal adverse events including nausea, vomiting, and constipation, which may be severe in some individuals. These compounds are not recommended in patients with a personal or family history of medullary thyroid carcinoma or MEN 2.

Contraindications (based on compound mechanism and trial exclusion criteria): personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia syndrome type 2; active malignancy with potential receptor expression; severe or uncontrolled gastroparesis; history of serious hypersensitivity to biologic therapeutics; pregnancy and breastfeeding; severe renal or hepatic impairment.

Common adverse events reported in Phase 1 and Phase 2 trials: nausea, vomiting, constipation, consistent with GLP-1 receptor agonist pharmacology. Long-term safety data in large populations are not yet available.

Weight regain: weight regain after discontinuation of GLP-1-class pharmacotherapy has been documented in published extension studies for approved compounds in this class. Maritide's post-dose weight maintenance signal from Phase 1 has not been confirmed in Phase 3 populations.

This is not a complete list of risks. Full information for the investigational compound is available through the MARITIME clinical trial consent process at ClinicalTrials.gov.

Additional Questions

What is the difference between AMG 133, maritide, and maridebart cafraglutide?

These are all names for the same compound at different stages of development. AMG 133 is Amgen's internal development code. Maridebart cafraglutide is the International Nonproprietary Name (INN) assigned to the compound. Maritide is a shortened name used in reporting and in this article. All three refer to the same bispecific antibody-peptide conjugate combining GIPR antagonism and GLP-1 receptor agonism.

Can I get maritide from a compounding pharmacy?

No. Maritide is an Amgen proprietary investigational biologic. There is no legitimate source for compounded maritide, and any product sold online or through gray-market channels as maritide, AMG 133, or maridebart cafraglutide has not been manufactured, tested, or approved by the FDA. The compound's antibody-drug conjugate structure is not reproduced through standard compounding processes. Seeking access outside of clinical trials carries serious risks.

Will maritide be available by prescription in the future?

Possibly, if the Phase 3 MARITIME trials produce positive efficacy and safety data and Amgen submits a successful NDA or BLA to the FDA. No approval timeline can be projected with certainty; Phase 3 completion, data analysis, and FDA review typically require several years. As of April 2026, no approval date has been announced.